Advances in the Management of Hypercholesterolemia - Episode 14
Howard Weintraub, MD: You brought up a very good point, and I agree with what you said. Certainly, having an LDL [low-density lipoprotein] of 72 vs. 69 mg/dL would be good in the mind of a computer but not in the mind of a plaque. You brought up acute coronary syndromes. There have been several reports looking at the early institution of vigorous LDL reduction, particularly in the non-statin-naïve patients, and starting them on either evolocumab or alirocumab soon after the event. There’s a bit of a language differential between the American and European guidelines. Our prevention group sees a lot of patients, and we are asked to see a lot of patients who come in with PCIs [percutaneous coronary interventions]. It was a decision by the heads of the catheterization laboratory and cardiology to have them get prevention consults before they leave. That is so they don’t become part of a revolving wheel of individuals coming in, having a little done medically but not enough, and then coming back a year later.
Thankfully, we at NYU Langone Health are allowed to have samples. In several cases, before the patient left—because we get a lipid profile when they come in—we have given them a shot of a PCSK9 inhibitor. Then we try to work with the patient and their primary care physician, or they’ll come back and see us and we try to get them on board to use a PCSK9 inhibitor. Along with adoption of the drug, there are also some other issues about early adoption. I find, as I’m sure you do, that there’s a bit of inertia.
We’d asked before whether you titrate or go right to the high dose. Even if the patient comes in and their LDL is 160 mg/dL, you and I know it’s unlikely that they’re going to get where they need to go with a statin alone. They may come close. They may reach the goal with ezetimibe. But the more common patient is someone who comes in with an LDL of 130 mg/dL, and they’re already on 40 mg of atorvastatin or 20 mg of rosuvastatin. The addition of ezetimibe is unlikely to get them down to a place that you and I would be comfortable with. These are individuals who would be well served—along with considering ezetimibe—to recognize that waiting 3 or 6 months for the LDL to come down on ezetimibe is going to be time wasted. How do you feel about that?
Alan S. Brown, MD, FACC, FAHA, FNLA: Systems turn good doctors into great doctors. If that system is to have anyone with an acute coronary syndrome whose LDL is still elevated get started on therapy before they leave the hospital, that’s reasonable to me. If they’re already on a statin and they come in with an LDL above 70 mg/dL, adding a PCSK9 inhibitor is perfectly reasonable. If that’s the way your system works, and you can make that happen, it’s great. Every step that requires another blood draw and titration reduces the chance that the patient is going to get adequately treated.
If you wait 6 weeks and have them see you in the office then, some of them won’t come back to your office. They may go elsewhere. If you add the ezetimibe, you wait another 6 weeks. You must have a certain sense of urgency after an acute event. You need to have a system in place to make sure people are adequately treated. I don’t have problem with another type of system in which everyone with acute coronary syndrome gets an appointment with prevention within the next 2 weeks and they get started on therapy as an outpatient, especially if the hospital says, “We don’t want to stock X, Y, or Z as an outpatient drug.” But there has to be some sort of system so the patients don’t get missed. As they have 2 or 4 visits, the number of people who are adequately treated drops off exponentially. You have the patient’s attention when they’re in the hospital too.
A final thing is that there has been some suggestion over many years—I’m not sure if it’s true—that when we start something in the hospital, everyone is afraid to stop it. That’s why people are taking Lanoxin [digoxin] for 20 years for PAC [premature atrial contractions].
Howard Weintraub, MD: That’s exactly what I was thinking.
Alan S. Brown, MD, FACC, FAHA, FNLA: Some data suggest that may not be true, but there is some inertia behind starting it in the hospital that may make the patient more likely to stay on it.
Howard Weintraub, MD: To elaborate on what you just said, in many cases, the cardiologist who attended to the patient in the hospital is an interventionalist who doesn’t have much of an outpatient presence. The patient goes back to their primary physician, and they look at the patient’s lipid-lowering and say, “You went into the hospital on 20 mg of Lipitor and you’re coming out on 40 mg of Lipitor.” Theoretically, the patient is getting high-dose, high-intensity statin. The primary care physician says, “Look, these smart guys in the hospital thought that this was all you needed. Who am I to say this is wrong?”
There are multiple ways to approach this. We are fortunate in that we have a large, dedicated prevention section. Also, having a dedicated fellow working with us has really been a godsend in this regard, and it makes it very interesting. That, and being able to have a little refrigerator in our office with a mini supply of alirocumab and evolocumab makes it much easier. Even if you give them the drug and they don’t get it for 2 or 3 weeks, most PAs [prior authorizations] are accomplishable within that amount of time.
The only obstacle is when it’s contested. The patient doesn’t show up in prevention, and you’re left with a patient getting dropped. The way we look at it is, if you don’t start it in the hospital, you’re going to lose even more. We are trying this out. We’re doing it on our own. There were some institutions doing it on a trial basis, but we’ve been doing this as a course of good practice. You have to work it out however you can. If you cajole them back to the prevention section for a visit afterward and our note goes out with the catheterization note, we speak to the patient and they know what we’re recommending. We give them their lipid numbers before they leave the hospital, including an A1C [glycated hemoglobin]. We always draw an LP(a) [lipoprotein (a)] in someone appropriate. We have our NP [nurse practitioner], prevention fellow, or 1 of us if necessary, follow up with the patient, particularly if it’s high.
We need to do whatever we can to break the cycle of where things are going. You and I teach. We see people who have had stents and MIs [myocardial infarctions], and they show up again on exactly the same medicines they were on when they came in for the first go-around. To me, this is almost as bad as the patient who’s still smoking, whose blood pressure is untreated, and whose A1C has been left to climb over 8 mg/dL. You’re looking at this going, “Oh my God.” But this is something we have the ease of being able to treat. The nice thing about it is, it’s not another pill that the patient takes.
Transcript Edited for Clarity